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A shake of the head to a wink of the anus
  1. O M Jones1,
  2. A F Brading2,
  3. N J McC Mortensen3
  1. 1Department of Pharmacology, Mansfield Road, Oxford OX1 3QT, UK and Department of Colorectal Surgery, John Radcliffe Hospital, Oxford OX3 9DU, UK
  2. 2Department of Pharmacology, Mansfield Road, Oxford OX1 3QT, UK
  3. 3Department of Colorectal Surgery, John Radcliffe Hospital, Oxford OX3 9DU, UK
  1. Correspondence to:
    O Jones;
  1. M A Kamm4
  1. 4St Mark's Hospital, Watford Road, Harrow HA1 3UJ, UK;

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We read the case report of Malouf and Kamm (Gut 2001;48:728–9) with interest. However, we disagree with some of the science and suggest an alternative explanation for their findings.

Firstly, there is much data to suggest that sympathetic innervation of the internal anal sphincter is in fact excitatory. The paper that they cite1 (from their own institution) showed that noradrenaline, the principal postganglionic neurotransmitter of the sympathetic nervous system, caused contraction of this tissue in vitro. Operative in vivo studies of presacral nerve stimulation have indeed been contradictory, showing both an increase2 and decrease3 in internal anal sphincter tone; this probably reflects little more than differences in stimulation parameters. However, sympathetic blockade effected either by infusion of the α adrenoceptor antagonist phentolamine4 or by high spinal anaesthesia5 produces a significant fall in internal anal sphincter tone. This is evidence of tonic, excitatory, sympathetic innervation of the internal anal sphincter, not of “extrinsic sympathetic drive which relaxes the sphincter”, as described by Malouf and Kamm.

Secondly, acetylcholine relaxes internal anal sphincter in vitro,6 an action blocked both by atropine and nitric oxide synthase inhibitors. This implies that acetylcholine, the principal postganglionic neurotransmitter of the parasympathetic nervous system, is inhibitory and acts via muscarinic receptors and its effects are mediated by nitric oxide. Low spinal anaesthesia has little effect on anal canal resting pressure, suggesting that there is negligible tonic parasympathetic discharge to the internal anal sphincter.5 We are not aware of any convincing data that enable Malouf and Kamm to make the unreferenced statement that there is “normal extrinsic parasympathetic excitatory [sic] drive to the internal anal sphincter”.

Finally, the anal canal normally remains closed at rest because of the tone of the internal anal sphincter, which contributes around 80% of resting anal pressure.7 Most of this contraction is attributable to intrinsic myogenic tone although there is some tonic sympathetic discharge, as outlined above. Malouf and Kamm describe the anus of a spinal cord injured patient as having “gaped after digital examination for several minutes” and state that this might reflect loss of “normal extrinsic parasympathetic excitatory [sic] drive to the internal anal sphincter”. A much simpler, and pharmacologically correct, explanation would be that digital examination of this patient evoked the rectoanal inhibitory reflex and induced internal sphincter relaxation. Indeed, we would dispute that normally “the anal canal remains closed before, during, and after examination”. When the fingertip passes into the rectum of a non-spinal injury patient, a definite relaxation of the internal anal sphincter is often felt. This is not normally sustained for minutes, and it is this abnormality that is interesting in the case they report. High resting pressures are often seen in spinally injured patients and many of them use digital rectal stimulation to aid defecation.8


Author's reply

I am grateful to Drs Jones, Brading, and Mortensen for their comments. I agree that the extrinsic sympathetic innervation to the internal sphincter is predominantly excitatory, and that the parasympathetic extrinsic innervation causes internal sphincter relaxation. As mentioned in their letter, our own in vitro studies have demonstrated this convincingly. That we stated the reverse in our “Gut file” case report was a simple error, and I appreciate the correction.

The main point of the report however remains the original description that gaping of the anal canal, with failure to return to its state of normal resting tone, after simple examination may reflect underlying extrinsic neurological damage. Although it is true that approximately 80% of the resting anal tone is contributed to by intrinsic myogenic activity of the internal sphincter in health, we do not know how loss of the normal extrinsic nerve supply may alter smooth muscle function. Damage to the extrinsic nerve supply affecting the sympathetic or parasympathetic components may also result in altered sphincter control and behaviour.

I doubt that the rectoanal reflex was the cause of this patient's sustained anal relaxation. In healthy subjects this reflex requires rectal distension, which does not occur during simple digital examination. Furthermore, any slight relaxation that might occur during digital examination is normally short lived and ceases when the finger is withdrawn. As stated in their letter, we believe it is this failure of the sphincter to return to a closed state that may be a pointer to underlying neurological disease.

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